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ACUTE EXPOSURE INFORMATION

1. ORAL
   1. Red or amorphous phosphorus is nonvolatile, insoluble, unabsorbable and, therefore, nontoxic when ingested. However, it may contain traces of yellow phosphorus (up to 0.6%) and large ingestions may result in adverse effects.
   2. Black phosphorus is the inert, nontoxic allotropic form of elemental phosphorus.
   3. This document will focus on yellow phosphorus unless otherwise noted.
   4. Systemic phosphorus poisoning may occur following oral, inhalational, and dermal exposure.
   5. Toxicity is enhanced when phosphorus is dissolved in solvents, e.g., alcohol, digestible fats, oils.
   6. Clinical effects following ingestion have classically been divided into an initial gastrointestinal (GI) stage, followed by a relatively asymptomatic period, lasting from 8 hours to several weeks, and terminating in acute liver and renal failure with metabolic derangements.
   7. Ingestion is usually followed by vomiting, which is "smoking", luminescent, and with a garlicky odor. Stools may also be "smoking" and luminescent.
   8. In clinical practice, patients present with symptoms referable to the GI tract (nausea, vomiting, abdominal pain, diarrhea, hematemesis), CNS (restlessness, irritability, drowsiness, lethargy, weakness, delirium, stupor, coma, seizures), or both, with respective mortality rates of 23%, 73%, and 47%. Cardiovascular collapse may accompany the presenting GI symptoms.
   9. Death in the first 12 hours is usually the result of peripheral vascular collapse. Death within 24 to 48 hours may ensue from peripheral vascular collapse and is frequently accompanied by acute renal failure. Deaths within 48 to 72 hours may result from peripheral vascular collapse or cardiac arrest with hepatic and/or renal failure. Seizures may also be evident.
   10. Death usually occurs 4 to 8 days after ingestion, but may be delayed. Ingestions of 50 mg or 1 mg/kg may be fatal.
   11. Early hypoglycemia has a grave prognosis. Survival for three or more days is a good prognostic sign.

2. INHALATION
   1. Acute inhalational exposure to phosphorus fumes would be expected to produce ocular upper respiratory irritation and possibly delayed onset of noncardiogenic pulmonary edema.
   2. Chronic industrial inhalational exposure to phosphorus fumes has resulted in symptoms that include bronchitis, anemia, cachexia, and mandibular necrosis ("phossy" or "Lucifer's jaw").
   3. Phosphorus that is absorbed through inhalation can result in acute hepatic damage and systemic phosphorus poisoning.

3. DERMAL
   1. Dermal exposure may result in severely painful, necrotic, partial to full thickness yellowish color burns from chemical and thermal effects with a garlic-like odor. This is likely to occur if it reaches the ignition temperature (44 degrees Celsius or 111 degrees Fahrenheit). Second and third degree burns can occur within a few minutes to hours.
   2. Phosphorus absorbed from damaged skin may result in acute systemic phosphorus poisoning.

4. CHRONIC
   1. Occupational poisoning may produce necrosis of the mandible, called "phossy jaw", cachexia, anemia and general disability.

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